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ERV FAQ: What is the "case for common descent" from ERVs?

Here is a brief overview. Much more detail can be found here,
Three Layers of Endogenous Retroviral Evidence for the Evolutionary Model.
Further FAQ entries will go into into the following points in more depth.


1. Retroviruses replicate by invading the cells of host organisms, converting their RNA genomes into DNA, and inserting (integrating, in the jargon) the DNA into the DNA of the host cell. The integrated DNA is called a "provirus". The host cell then "reads" the provirus, converting it back into RNA, resulting in the production of more viruses.

2. Retroviruses tend to target certain types of cells. Their "environment" proteins tend to be specialized to attach to the surfaces of these cells.

3. The insertion is made by a retroviral enzyme called integrase. While certain retroviruses can show a general tendency to insert their DNA in certain types of regions in a host cell's DNA, they do not target specific points (loci). This means that in an infected individual, not all cells will be infected, and in those that are, the retroviral integration will be in a different place or places in the DNA of each cell.

4. We find, in the genomes of creatures such as ourselves and chimpanzees, inherited structures that appear to be broken retroviral insertions. Some are more complete than others, but many have the full set of genes that would be necessary for a complete retrovirus, were they not faulty. We call these structures endogenous retroviruses (ERVs). Unlike the case where each cell is individually infected, they appear in the exact same spots in the DNA of every single nuclear cell (cells with nuclei containing DNA).

5. Although certain components of some ERVs perform functions in the host, some even being essential in some species, no complete ERVs are functional. Design, as an explanation for ERVs, does not make any sense. A designer would have no need to include specifically retroviral genes in its designs, which now do nothing, or may even cause harm. There would also be no need to design in non-functional traces of the action of integrase, traces of which are present in ERVs.

6. The only explanation that makes any sense is that ERVs are the result of retroviral insertions into germ-line DNA - egg cells or sperm cells, followed by reproduction and consequent cell division. Cell division will duplicate the ERVs in the same positions in the DNA of every cell. Separate, parallel infection would not infect every cell, and the proviruses would end up in different locations, comparing one infected cell with another.

7. All human beings have some 200,000+ ERV and ERV fragments in the DNA of every one of their cells. Most of them are in identical DNA locations going from cell to cell, and person to person. This means that we all share common ancestors - the ancestors that first acquired each of the germ-line retroviral infections.

8. All human beings and chimpanzees have some 200,000+ ERV and ERV fragments in the DNA of every one of their cells. Most of them are in precisely corresponding DNA locations going from cell to cell, and individual to individual. This means that we all share common ancestors - the ancestors that first acquired each of the germ-line retroviral infections. See  http://www.evolutionarymodel.com/ervs.htm#Amount_of_Shared_ERVs


27 comments:

  1. It could very well be that current science has cause and effect up-side-down: we are not made of viruses, but viruses are made of us. For a major part, the genomes of all organisms exists of what we now call TEs (transposable and transposed elements). We have found out that they fulfill many crucial functions in regulating gene expression and keeping the genome together. I prefer to call TEs after their functions in the genome: variation-and-integrity-assuring genetic elements (VIGEs). In my paper of 2009, I describe how we are able to understand the origin of RNA viruses from VIGEs commonly referred to as ERVs. In my 2013 paper, I demonstrate that the syncytin gene does not originate in the genes of an RNA virus (ERV-W), as it is generally believed, but that a particular VIGE (gag-pol element know as an endogenous retrovirus) picked up the syncytin gene from the genome to become a provirus. There is ample evidence for this view and summarized in my papers. In other word, we see the for-runners of full blown RNA viruses develop ("evolve") in our genomes. This is the best explanation for the existence of RNA viruses. That VIGEs are an integral part of our designed genomes is clear from DNA-histon binding rules that their sequences tightly adhere to. Open minded people will follow up on this novel idea.

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    1. Peer, here is why ERVs are concluded to be the inherited remnants of retroviral integrations in germ-line DNA. http://barryhisblog.blogspot.com/p/why-do-virologists-and-geneticists.html

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    2. You are not the only one who uses your sciency-sounding acronym. But how does it account for The koala retrovirus/ERV, KoRV?

      "Of 39 distinct KoRV proviral loci examined in a sire–dam–progeny triad, all proved to be vertically transmitted and endogenous; none was exogenous. Of the 39 endogenous KoRVs (enKoRVs), only one was present in the genomes of both the sire and the dam, suggesting that, at this early stage in the retroviral invasion of a host germ line, very large numbers of ERVs have proliferated at very low frequencies in the koala population. (Proliferation of Endogenous Retroviruses in the Early Stages of a Host Germ Line Invasion)"


      In other words, the progeny had inherited copies of KoRV in 39 different locations in its DNA. All of these corresponded to an ERV in one parent or the other, but only one of them was common to all three. The remaining 38 were in one parent, or the other, but not both. Proof that these were not “designed” into the koala genome, but acquired, either by direct endogenization, or by endogenization in an ancestor.


      http://barryhisblog.blogspot.com/p/the-koalas-tale.html

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    3. The Koala retrovirus did not originate in Koala, Barry. It has its origin in Asia, in rodents. And it is, just like all RNA viruses, derived from an ERV, not the other way around. The origin of RNA viruses is in the genome, in genetic elements we know as ERVs, but which should be renamed VIGEs (variation and integrity assuring genetic elements). I am oppssing the mainstream opinion on the origin of RNA viruses since about 10 years, now, and all the recent evidence is confirming the VIGE-first-hypothesis, i.e. origin in the genome as exogenization events of transmutated ERVs (which picked up parts of the genome to become shuttle vectors).

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    4. So KoRV wasn't designed into the koala genome? You have just destroyed your own "argument", Anon. :P

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    5. Peter Borger... You are the Young Earth Creationist Peter Borger right?

      You seem well informed ehough... so surely you realise that the mere presence of LTRs flanking an ERV is concrete evidence that this sequence was once reverse transcribed from RNA to DNA? LTRs are about as convincing a piece of evidence you could ever hope to find that an ERV at a given location wasn't always there.

      We have thousands of ERVs which are flanked by LTRs which are shared in identical locations with Chimpanzees.

      The ONLY reasonable explanation for this Peter is that these infections happened in a common ancestor and were inherited by both humans and chimpanzees.

      If you want to believe that all viruses ultimately come from ERVs, you could do that (although Occam's Razor says we should rule this out). What you can't deny though - if you intend to be honest with yourself - is that thousands of shared ERVs with LTRs provide concrete evidence for common ancestry regardless of where you think ERVs ultimately originated from.

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    6. Ultimately, all RNA viruses kan be tracked back to an escaped ERV (which Peer coined VIGEs) somewhere in a genome. The Koala retrovirus can thus be tracked back to an Asian population of rats. The RNA world is just a story devoid of any evidence. RNA viruses have their origin in genomes. We can even determine what parts they took from those genomes. The RSV, for instance, took a part of the SRC gene and turned into an onco-RNA-virus. This is only reasonable explanation for the existance of RNA viruses. Thousands of shared retroviruses my simply reflect the positions where the VIGEs originally located or due to a mechanism now no longer in operation.

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    7. @Barry,
      no I did not destroy my own argument. I simply say that the origin of all RNA viruses is in genomes. Then, they may spread horizontally through the animal kingdom (as happened with the "Koalavirus", with HIV, with Influenza, etc).

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    8. "What you can't deny though - if you intend to be honest with yourself - is that thousands of shared ERVs with LTRs provide concrete evidence for common ancestry regardless of where you think ERVs ultimately originated from."

      There are thousands of RNA- and protein-coding genes present in humans not found in chimps. They effectively falsify common descent and demonstrate we must look for other explanations to understand shared ERVs and LINEs. In my opinion, genes, programs and variation-inducing elements were frontloaded in primordial organisms. All that is required for variation, adaptation and speciation is reshuffling of code.

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    9. Peer, you have Koala populations with no endogenous KoRVs. They are not designed features. (And my information is that it closely resembles the gibbon ape leukemia virus (GALV). See my comments and link above.

      And yes, humans an chimps are different species. That's because there are differences between their genomes! To say they falsify common descent is nonsense.

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    11. Indeed, Barry, there are Koalas with no endogeneous KoRVs. But does that address the origin of the KoRV? No. The KoRVs can be tracked back to an Asian population of rodents (to my knowledge) or to GALV in Gibbons. Still, the origin of the RNA virus that became the KoRV was in the genome of another eukaryote. I do not deny horizontal spread of RNA virusen. I hypothesize that ERVs are VIGEs, and part of a designed mechanism to induce rapid variation, adaptation and speciation. Left alone, such VIGEs are able to mutate into RNA viruses.

      And yes, the difference between chimp and man is approx 2500 genes and not 1-2% nucleotides in shared genes (as it is commonly believed). The real difference is found in unique information, and that is 2500 genes! This makes an evolution-did-it-story highly unlikely. So, we are in need of an alternative explanation of shared ERVs. I gave a plausible scientific explanation in the VIGEs-first hypothesis.

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    12. Peer's trick is to keep repeating his hypothesis, with slightly different words, as evidence his hypothesis is true (begging the question.) "The Koala retrovirus...just like all RNA viruses, derived from an ERV, not the other way around." An EXTRAORDINARY hypothesis that is not evidence, not a fact, not an observation... it is supported by no evidence but, like all extraordinary hypotheses, requires extraordinary evidence.

      We have seen retroviruses incorporated into genomes. That makes it an ordinary hypothesis supported by observation. You are trying to pass off an extraordinary hypothesis and, when asked for evidence, you support by repeating your hypothesis with different wording.

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    13. Frank, I do not have a trick...I do science. I have been thinken very long about the genome and what it contains. I now know how it works and what it means. My VIGEs-First hypothesis is the better explanation for the evolution of RNA viruses and it also explains the syncytin locus much better than the mainstream view.

      It does not matter how many retroviruses have been observed invading the genome (there are not many observations, however). It does NOT address the origin of retroviruses. I will repeat my VIGE-Firsts hypothesis as long as it is required, because it will eventually be accepted and increase our knowledge on RNA viruses, their origin, and how to beat them. That is my aim.

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    14. The extraordinary evidence Frank asked for is found in the RSV (rous sarcome virus), in the HIV (human immuno deficiency virus), and the influenza virus. Their virulent genes can simply be tracked back in the genomes of the organisms they escaped from. RSV picked up half of the SRC gene, which is a proto-oncogene, present in all higher mammals. SRC is molecular regulator of the cell cycle, and the whole gene specifies both on- and off-switches to control cell divisions. Unfortunately, an ERV (better: gag-pol element) fused with only one exon specifying the on-switch only. No wonder that the RSV is known as a notorious oncovirus. Likewise, influenza virus (IV) is a fused ERV (better: gag-pol element) with part of a eukarytotic neuramidase gene (enzymes that split certain aminoacids, but IV uses is as a capsid component) and HIV uses a sequence present in CXCR gene family to dock to CCR5 (and to enter immune cells). As you can see, the "VIGEs-first hypothesis" has loads of explanatory power.

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    15. "Still, the origin of the RNA virus that became the KoRV was in the genome of another eukaryote." Not in evidence. It is infectious retroviruses that cross species. They may then endogenize. They cannot endogenize repeatedly in specific locations. This fact is in evidence. Also in evidence is the fact that inheritance places the same genetic material in the same loci. As Frank says, Peer, all you are doing is repeating the same unsupported hypothesis and you are ignoring the actual evidence for common ancestry from endogenization.

      And apart from lacking evidence, your hypothesis makes no sense. An all-powerful, all-knowing absolutely intelligent agent designing genomes so that they can take uncontrolled bits of genomes out and insert them in uncontrolled loci in mostly somatic cells of individuals of the same or different species, in the hope that they will occasionally endogenise and occasionally confer a fitness advantage? This is patent nonsense. What advantage does KoRV confer on koalas? The only known effect is oncogenesis. Why couldn't your unnatural genetic engineer have at least used CRISPR?

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    16. The Koala virus is tertiary. First, you had a designed non-virulent gag-pol element present in the genome of an Asian organism unrelated to the Koala, most likely a rat or a primate (see above). Second, this gag-pol element acuired a few sequences from the genome where it resided and thus transformed into an RNA virus that was able to shuttle between the interior and exterior of cells. Third, the RNA virus acquired virulence genes to shuttle between organisms and invaded the germline of the Koala, where it now causes disease. It is as easy as the VIGE-first hypothesis. It is so explanantory, so elegant. It must be true.

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    17. So a gag-pol element was designed into a gibbon or a rat so that it would transform into a provirus, generate exogenous retroviruses and transfer to koalas - just to give koalas cancers and endogenize in them? Do you even read what you write?

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    19. This comment has been removed by a blog administrator.

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  2. Peer, I have preserved your comments, but they will not appear here until you make an adequate response concerning the CMI statement of faith.

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  3. Nice trick @Barry. You @Barry are the only person here who said anything about an "An all-powerful, all-knowing absolutely intelligent agent" @Peer never said anything, so when you cannot refute him you removed his comments and call him a creationist. Very honest of you....

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    1. This was Peer's thesis. Peer blogs for Creation Ministries International, one of the most notorious creationist organisations. I repeatedly asked him about his attitude to their "statement of faith", and he has repeatedly declined to answer. This goes directly to his trustworthiness as an honest and objective commentator.

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    2. No I read the exchange, he never once mentioned a God. Consider -

      A mass murderer correctly teaches algebra to some students. You come along and say, well algebra must be false because you are a mass murderer. This is what we ( <- philosophers) call "the Genetic Fallacy".

      Let us suppose that Peer is a young earth creationist (YEC)... Who cares? It has nothing to do with what he has been discussing. What he has said is not dependent on "YEC" being true.

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    3. RAZA, you are trying to make an argument using an extremely poor analogy (is there a name for such a fallacy?) But your fallacy is informative. Algebra, like all mathematics, is dependent on a universally agreed set of axioms and rules of combination. A mass murderer who applies these may still do valid algebra. But what about someone who has sworn to ignore the methods of science if they produce an outcome that contradicts their pre-conceived beliefs? And what if they refuse to even admit to such an attitude? How honest and reliable can we expect them to be? Certainly, I would be happy to continue discussing the evidence and attendant reasoning with Peer, but I would like him to clarify this matter first. It is not much to ask.

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    4. There is a fallacy called "faulty analogy" not sure if that's the one you wanted.

      " But what about someone who has sworn to ignore the methods of science if they produce an outcome that contradicts their pre-conceived beliefs?" This describes the scientists like Francis Crick who wrote " Biologists must constantly keep in mind that what they see was not designed, but rather evolved." (from What Mad Pursuit (1990), 138) In spite of the evidence of intelligent design, biologist must "remind themselves" it is not - why? Because they already have a preconceived notion that there is no design [in spite of the evidence against this].

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    5. And the evidence against this is - what?

      And a reminder - this page is about the evidence for common descent from ERVs. Can you propose a "design" explanation for commonly located ERVs, bearing in mind what I say here http://barryhisblog.blogspot.com/p/in-science-we-apply-principle-of.html ?

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